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Biology of Reproduction 63, 1219-1228 (2000)
© 2000 Society for the Study of Reproduction, Inc.


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Leptin in Pregnancy

Michael C. Henson,a,b,c,d, and V. Daniel Castracanee,f

a Departments of Obstetrics and Gynecology, b Physiology, and c Structural and Cellular Biology, Tulane University Health Sciences Center, New Orleans, Louisiana 70112-2699 d Tulane Regional Primate Research Center, Covington, Louisiana 70433-8915 e Department of Obstetrics and Gynecology, and f the Women's Health Research Institute of Amarillo, Texas Tech University Health Sciences Center, Amarillo, Texas 79106-1797

Leptin is a polypeptide hormone that aids in the regulation of body weight and energy homeostasis and is linked to a variety of reproductive processes in both animals and humans. Thus, leptin may help regulate ovarian development and steroidogenesis and serve as either a primary signal initiating puberty or as a permissive regulator of sexual maturation. Perhaps significantly, peripheral leptin concentrations, adjusted for adiposity, are dramatically higher in females than in males throughout life. During primate pregnancy, maternal levels that arise from adipose stores and perhaps the placenta increase with advancing gestational age. Proposed physiological roles for leptin in pregnancy include the regulation of conceptus growth and development, fetal/placental angiogenesis, embryonic hematopoiesis, and hormone biosynthesis within the maternal-fetoplacental unit. The specific localization of both leptin and its receptor in the syncytiotrophoblast implies autocrine and/or paracrine relationships in this endocrinologically active tissue. Interactions of leptin with mechanisms regulating pre-eclampsia and maternal diabetes have also been suggested. Collectively, therefore, reports suggest that a better understanding of the regulation of leptin and its role(s) throughout gestation may eventually impact those causes of human perinatal morbidity and mortality that are exacerbated by intrauterine growth retardation, macrosomia, placental insufficiency, or prematurity.

First decision: 3 April 2000.

1 Correspondence: Michael C. Henson, Department of Obstetrics and Gynecology (SL-11), Tulane University Health Sciences Center, 1430 Tulane Avenue, New Orleans, LA 70112-2699. FAX: 504 584 1846; michael.henson{at}tulane.edu




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